Dysregulation of long non-coding RNA SNHG12 alters the viability, apoptosis, and autophagy of prostate cancer cells by regulating miR-195/CCNE1 axis.

This study aimed to explore the role and mechanism of lncRNA small nucleolar RNA host gene 12 (SNHG12) in the development of prostate cancer (PCa). The expression of SNHG12 in the serum of PCa patients as well as PCa cells was determined, and then we investigated whether SNHG12 could act as a competing endogenous RNA (ceRNA) to mediate the development of PCa. Furthermore, the association between SNHG12 and activation of the PI3K/AKT/mTOR pathway was explored. SNHG12 expression was up-regulated in the serum of PCa patients as well as PCa cells. High expression of SNHG12 resulted in a poor prognosis of PCa patients. Moreover, suppression of SNHG12 inhibited viability and promoted apoptosis and autophagy of LNCaP cells. Furthermore, SNHG12 was found to act as a ceRNA to regulate the expression of Cyclin E1 (CCNE1) by sponging miR-195. Lastly, suppression of SNHG12 inhibited the activation of PI3K/AKT/mTOR pathway. Our results revealed that up-regulation of SNHG12 promoted the viability and inhibited apoptosis and autophagy of PCa cells by regulating CCNE1 expression by sponging miR-195. Moreover, activation of PI3K/AKT/mTOR pathway is a key downstream mechanism regulating SNHG12-mediated the development of PCa. Our findings provide an experimental basis for targeted therapy of PCa.